This research is concerned with the neurophysiological and anatomical correlates of collateral sprouting of uninjured axons in response to adult mammalian spinal cord injury, and the relationship of this sprouting to recovery of function. Partial deafferentation by dorsal rhizotomy or lesions of descending pathways have been shown anatomically to produce collateral sprouting of intact dorsal root afferents. Extracellular, neurophysiological recording methods will be used to investigate the nature and time course of changes in the properties of spinal cord neurons as a result of this sprouting. In animals subjected to dorsal rhitzotomy, attention will be directed to changes in the sonatotopic organization of the dorsal horn following partial deafferentation. Lesions of descending pathways will be performed either by spinal cord hemisection or by aspiration of sensorimotor cortex. In these animals, the grey matter of the L7 segment will be examined for changes in somatotopy, receptive field size, and the size of the region giving rise to short latency responses to sural nerve stimulation. To explore further the phenomenon of collateral sprouting, the technique of intracellular recording and HRP labeling of primary afferents will also be used. Single afferents whose response properties have been characterized will be labeled in normal animals and in animals with lesions thought to produce sprouting of those afferents. Labeled axons will be examined for differences between groups in the density of synaptic terminals, and in the extent of terminal arborizations.